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Breathless: How blood-oxygen levels regulate air intake

New York, April 22 (IANS) Researchers have unravelled the elusive process by which clusters of sensory cells in the carotid arteries detect oxygen levels in the blood as it flows toward the brain.

This “tasting of oxygen” by sensory cells is the first step in regulating blood-oxygen levels.

The cells translate that taste test into signals, sent through the carotid sinus nerve to stimulate or relax breathing rates, said the team that includes an Indian-American scientist.

“After a lengthy search, one that began almost 90 years ago, we were able to identify the long-sought oxygen sensor,” said study senior author Nanduri Prabhakar from the University of Chicago.

The primary blood-oxygen sensor is the enzyme heme oxygenase-2. “This is the critical molecule. It is a crucial component of this process,” Prabhakar said.

When blood is adequately oxygenated, heme oxygenase-2 induces synthesis of the gaseous messenger carbon monoxide. This carbon monoxide initiates a chain of events.

It stimulates production of cyclic guanosine monophosphate, activating protein kinase G.

Protein kinase G then adds a phosphate group to the enzyme, called CSE, blocking the generation of hydrogen sulfide, another gas messenger.

Inactivating CSE prevents the carotid body from sending out a nerve signal to increase air intake.

“When oxygen levels fall, there is no heme oxygenase-2 activity, and no production of carbon monoxide,” Prabhakar explained.

The carotid bodies instead produce abundant hydrogen sulfide which activates nerve signals.

This increases breathing, heart rate and blood pressure. “Hydrogen sulfide goes up as oxygen level goes down,” he said.

While adequate oxygen in the blood inhibits nerve signals, an oxygen shortage – caused by stresses such as exercise, lung disease, sleep apnea or thin air at high altitudes – sets off an alarm, promptly sending the signal to breathe to the central nervous system.

An inadequate response to hypoxia can lead to serious consequences, such as hypertension and pulmonary oedema at high altitude.

The study was published in the journal Science Signalling.

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